Abstract
Organisms need to adapt to the ecological constraints in their habitat. How specific processes reflect such adaptations are difficult to model experimentally. We tested whether environmental shifts in oxygen tension lead to events in the adult newt brain that share features with processes occuring during neuronal regeneration under normoxia. By experimental simulation of varying oxygen concentrations we show that hypoxia followed by re-oxygenation lead to neuronal death and hallmarks of an injury response, including activation of neural stem cells ultimately leading to neurogenesis. Neural stem cells accumulate reactive oxygen species (ROS) during re-oxygenation and inhibition of ROS biosynthesis counteracts their proliferation as well as neurogenesis. Importantly, regeneration of dopamine neurons under normoxia also depends on ROS-production. These data demonstrate a role for ROS-production in neurogenesis in newts, and suggest that this role may have been recruited to the capacity to replace lost neurons in the brain of an adult vertebrate.
Article and author information
Author details
Ethics
Animal experimentation: The protocols were performed in accordance with EU regulations and were approved by local ethics committee (Permission number N429/12).
Reviewing Editor
- Alejandro Sánchez Alvarado, Stowers Institute for Medical Research, United States
Publication history
- Received: April 30, 2015
- Accepted: October 19, 2015
- Accepted Manuscript published: October 20, 2015 (version 1)
- Version of Record published: December 16, 2015 (version 2)
Copyright
© 2015, Hameed et al.
This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.
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